**5. History and examination**

tenocytes produce collagen earlier than those of the endotenon. Tenocytes of the endotenon produce large and more mature collagen than epitenon cells. In any event, both endotenon and epitenon tenocytes establish an extracellular matrix and internal neovascular network. Intrinsic healing results in improved biomechanics within the sheath, including tendon gliding. Movement of the tendon within the sheath improves synovial circulation and therefore the

Extrinsic healing involves the invasion of fibroblasts and inflammatory cells into the site of injury from the surrounding synovium, paratenon and tendon sheath [7, 14]. This produces scarring and peritendinous adhesions which may impair tendon movement, gliding and nutrition. It is thought that extrinsic healing predominates in the earlier stages of tendon healing. Extrinsic healing also predominates when tendons are immobilised after injury or repair. The extrinsic mechanism is activated earlier and is responsible for initial adhesions, the highly cellular collagen matrix and the high-water content of the injury site [7, 14]. The intrinsic mechanism then causes tenocytes from within the tendon to invade the defect and produce collagen which reorganises and aligns longitudinally to maintain fibrillar continuity and produce a

Careful surgical technique and initiation of early motion after surgical repair of flexor tendon injuries have been the main strategies for decreasing tendon adhesions after surgical repair. Recent research has concentrated on improving the healing response within the tendon whilst

• **Transforming growth factor β (TGF-β):** Chang and colleagues [16, 17] have shown that the isoform TGF-β1, present in small amounts in native tendon and its surrounding sheath, increase in production after tendon transection and repair. TGF-β1 has been postulated to contribute to fibrosis and therefore scarring [18, 19]. Shah and colleagues showed that the neutralising antibody to TGF-β was able to control scarring in rat dermal wounds [18, 19]. Chang et al. added to this by demonstrating that these antibodies were able to increase the total range of motion after flexor tendon repair in a rabbit model [20]. However, suppres-

• **Vascular endothelial growth factor (VEGF):** It is known that tenocytes secrete VEGF and is present in synovial fibroblasts [7]. After binding to its target, VEGF induces vasodilation [7]. VEGF mRNA levels are increased in flexor tendons after injury in the canine model [13]. These investigators are currently attempting to modify VEGF production to increase

• **Cell and molecular modulation:** Researchers have recently turned their attention to gene deletion strategies and gene therapy to modulate the healing process. Similar to inhibiting TGF-β, deletion of the TGF-β inducible early gene (*Tieg1*) resulted in decreased collagen I deposition in an *in vitro* model of tendon healing [23]. VEGF genes delivered by adeno-associated virus

sion of TGF-β has been shown to decrease strength of tendon repair [21, 22].

the vascular inflow to the blood supply of the healing flexor tendon.

decreasing the adhesion formation between the tendon and its sheath.

delivery of nutrients.

26 Essentials of Hand Surgery

**4.2. Extrinsic healing**

healed tendon [15].

**4.3. Research trends**

An accurate history and examination allows for planning of surgical approach. Though it is preferable for early tendon repair [30], immediate repair of a flexor tendon may be contraindicated in extensively contaminated wounds or those with substantial injury (involving two or more elements of skin, nerve, artery, vein, flexor tendons, extensor mechanism, bone or joint). Delayed presentation may also warrant surgical reconstruction of a flexor tendon due to proximal myostatic muscle-tendon retraction resulting inability to bring the proximal and distal stumps together.

It is important to perform a clinical examination of the traumatised hand before the administration of local anaesthesia to accurately identify and document neurologic or vascular injury [3]. Firstly, any volar laceration of the hand or wrist requires careful observation of the flexor cascade. In the normal cascade, each finger is slightly more flexed than the adjacent radial finger when the wrist is neutral or slightly extended.

To assess FDS, the FDP must be blocked from acting on the PIP joint. This is done by isolating the affected finger by holding all other fingers in extension and asking the patient to flex the PIP joint. By repeating the test against resistance, applied to the middle phalanx, partial lacerations of the tendon can be identified as it will elicit increased pain. FDP, responsible for flexion of the DIP, is tested in a similar manner to FDS. The middle phalanx is held in extension and the patient instructed to flex the DIP joint of each finger. Again, this can be done against resistance to identify partial tendon lacerations. FPL is tested by stabilising the proximal phalanx of the thumb and instructing the patient to flex the IP joint. However, a more reliable test of FPL function is using the 'O' sign where the patient is asked to make an O shape between their thumb and index finger. This O shape is only possible if the FPL is intact. This test is more reliable than asking the patient to flex the IP joint as there are trick movements that can cause a flicker of movement at the IP joint, causing diagnostic confusion.
